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Microbio Test 3 Review (ch 8, 10, 11) > Ch 11 > Flashcards

Ch 11 Flashcards

1
Q

What is normal microbiota?

A

permanently colonize the host and either cause no harm to the host or are beneficial to their host

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2
Q

transient microbiota

A

may be present for days, weeks, or months, more easily lost but are not harmful to the host

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3
Q

types of symbiosis

commensalism

A

one organism benefits
other is unaffected

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4
Q

types of symbiosis

mutualism

A

both organisms benefit

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5
Q

types of symbiosis

parasitism

A

one organism benefits and the expense of the other

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6
Q

How can normal flora cause disease?

A

Cause disease when in a new area of the body or host is immunocompromised aka opportunistic pathogens

Ex ecoli UTIs

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7
Q

primary infections

A

Acute infection that causes the
initial illness

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8
Q

secondary infections

A

Opportunistic infection after a
primary (predisposing) infection

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9
Q

Know a few factors that make us predisposed to disease

A

age
lifestyle
fatigue

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10
Q

What is a reservoir?

A

Continual sources of infection; living or nonliving

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11
Q

examples of reservoirs

humans

A

AIDS, gonorrhea

carriers may have subclincal (unapparent) infections or latent diseases

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12
Q

example of reservoirs

animals/ insects

A

rabies, lyme disease

zoonoses may be transmitted to humans from non-human reservoirs

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13
Q

examples of reservoirs

nonliving/ abiotic

A

botulism, tetanus

spores of clostridium species are found in soil and water

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14
Q

What are the 3 main routes of transmission?

A

direct

indirect

contact

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15
Q

direct transmission

A

droplet (aerosol)

body fluid exchange

fecal-oral

contact (STDs)

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16
Q

indirect transmission

A

foodborne

water-borne

fomite (inantimate object contact)

insect vectors/ animal zoonoses

environmental

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17
Q

contact transmission

A

direct: with infected/ reservoir

indirect: with inanimate object as intermediate

congenital: mother to fetus or to newborn at birth

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18
Q

What is a fomite?

A

indirect transmission

carry infectious microbes between hosts

ex. hypodermic syringe

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19
Q

transmission of arthropods

mechanical

A

arthropod carries pathogen on feet to host

host causes further contamination to self

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20
Q

transmission of arthropods

biological

A

pathogen reproduces in vector (insect) and is injected when insect bites host

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21
Q

What is MRSA?

A

methicillin resistant Staphylococcus aureus

resistant to the broad-spectrum antibiotics commonly used to treat it; can be fatal

mostly occurs in hospital aka healthcare-associated (MRSA or HA-MRSA)

older adults and people with weakened immune systems are at most risk of HA-MRSA

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22
Q

What are some factors that contribute to emerging and reemerging diseases?

A

genetic recombination

inappropriate use of antibiotics and pesticides

evolution of new strains

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23
Q

3 basic types of epidemiology.

A

descriptive

analytical

experimental

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24
Q

types of epidemiology

descriptive

A

collection and analysis of data

john snow

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25
Q

types of epidemiology

analytical

A

comparison of a diseased group and a healthy group

nightingale23e4

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26
Q

types of epidemiology

experimental

A

controlled experiments to learn how to prevent the spread of disease

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27
Q

What are features and examples of nosocomial infections?

A

aka healthcare associated infections

acquired during a hospital stay

affects 5-15% of all patients

reduced by following proper aseptic techniques during patient care and procedures

28
Q

examples of nosocomial infections aka healthcare associated infections

A

Urinary tract infections (UTIs)

surgical site infections

lower respiratory infections

29
Q

In what ways can opportunistic bacteria cause disease?

A

causes disease when in new area of body OR host is immunocompromised

ex e coli UTIs

30
Q

Know all terms involved in pathogenicity, virulence, and toxicity

A
31
Q

3 main characteristics of pathogens that determine virulence

infectivity

A

ability to establish focal point of infection

32
Q

** 3 main characteristics of pathogens that determine virulence**

invasiveness

A

ability to spread to adjacent tissues

33
Q

3 main characteristics of pathogens that determine virulence

pathogenic potential

A

degree to which potential can cause damage to host

34
Q

What are the 3 main routes of entry into the body?

A

mucous membranes

skin

oral-fecal route

35
Q

ID50

A

infectious dose for 50% of the test population

the amount of pathogen it takes for 1/2 of the individuals tested to become infected

36
Q

LD50

A

lethal dose (of a toxin) for 50% of the test population

the amount of toxin required to kill 1/2 of the individuals tested

37
Q

Do microorganisms have a preferred portal of entry? What does that mean?

A

most pathogens do have a preferred portal of entry

the portal of entry determines how many spores the bacteria will produce which will show how many bacteria are required to establish infection

38
Q

What are adhesins?

A

bind to receptors on host cells-INVASION

39
Q

ex of adhesions

A

glycocalyx: Streptococcus mutans

fimbriae: Escherichia coli

M protein: Streptococcus pyogenes

40
Q

What are some ways in which pathogenic bacteria have evolved ways to get around the immune system

A

cell wall: evasion
capsules: cover surface markers in their cell walls

enzymes: evasion and damage
hemolysins: lyse RBCs to release iron for pathogen use

41
Q

exotoxin

A

gram pos

proteins with 2 subunits (A-B)

heat unstability b/c these are proteins high temp denatures them

high toxicity

neutralized by antitoxin

small lethal dose

42
Q

endotoxin

A

gram neg

lipid

heat stability b/c high temp does not kill lipids

low toxicity

not easily neutralized by antitoxin

larger lethal does

43
Q

exotoxin
A subunit
B subunit

A

A subunit
does the damage / is toxic to the host cell

B subunit
extoxin is responsible for binding it to the target cell and transporting the A subunit into the target cell

44
Q

What are the general steps of entry of an A-B exotoxin?

A
  1. bacterium produces and releases exotoxin
  2. B (binding) component of exotoxin attaches to host cell receptor
  3. A-B exotoxin enters host cell by endocytosis
  4. A-B exotoxin enclosed in pinched-off portion of plasma membrane during pinocytosis
  5. A-B components of exotoxin seperate
    The A component alters cell function by inhibiting protein synthesis

The B component is released from the host cell

45
Q

membrane-disrupting exotoxins

A

Lyse host cells by making protein channels in the
host cell membranes

46
Q

What are superantigens

A

cause an intense immune response
due to a massive release of cytokines from host cells

  • Intense immune response occurs because they activate
    more immune cells than normal by binding non-
    specificall
47
Q

stages of disease

  1. incubation period
A

time between infection with a
microbe and the onset of
symptoms

48
Q

stages of disease

  1. prodromal period
A

first appearance of mild or nonspecific signs and symptoms of an illness

49
Q

stages of disease

  1. acute illness
A

most severe signs and symptoms

50
Q

stages of disease

  1. convalescence
A

the recovery period after an illness

51
Q

infection

A

invasion and growth of bacteria

52
Q

intoxication

A

Disease that results from a specific
toxin which may or may not have been produced
during the infection (some toxin are very stable!

53
Q

capsules: evasion
pathogens can avoid detection by host phagocytes by

A

covering surface markers on their cell walls

54
Q

capsules: evasion
is used by

A

Streptococcus pneumoniae, Bacillus anthracis Haemophilus influenzae

55
Q

capsules:evasion

Otherwise host phagocytes recognize pathogen cell
markers with receptors on their surfaces

A

Bacterial markers and host phagocyte receptors
interact to initiate phagocytosis

  • Once ingested: Lysosomes use a complex mixture of
    digestive enzymes and destructive oxygen radicals
    (e.g. super oxides) to destroy pathogens
56
Q

process of phagocytosis

A
  1. chemotaxis and adherence of microbe to phagocyte
  2. ingestion of microbe by phagocyte
  3. formation of a phagosome
  4. fusion of the phagosome with a lysosome to form a phagolysosome
  5. digestion of ingested microbe by enzymes
  6. formation of residual body containing indigestible material
  7. discharge of waste materials
57
Q

cell wall components: evasion
Many pathogenic bacteria have cell wall

A

factors that help
them evade the host’s immune system

58
Q

cell wall components: evasion

M protein

A

in Streptococcus pyogenes (also used in
adherence to host cells) helps resist phagocytosis

59
Q

cell wall components: evasion

Opa proteins

A

inhibits interactions between Neisseria
gonorrhoeae and T helper cells due to very tight packing
between bacterial cells mediated by Opa proteins

60
Q

cell wall components: evasion

mycolic acids

A

in (acid fast bacteria) Mycobacterium
tuberculosis and Mycobacterium leprae make it difficult
for phagocyte lysozomes to digest/destroy the pathogen

61
Q

enzymes: evasion and damage

some pathogenic bacteria produce enzymes that help them establish

A

an infection and/or cause damage to their host

62
Q

enzymes: evasion and damage
Coagulase

A

causes clotting of the blood; converts fibrinogen to fibrin which
coats the bacteria to help it evade phagocyte detection

63
Q

enzymes: evasion and damage

Kinases

A

ex. streptokinase
digests fibrin clots which allow pathogens to
escape from a clot and spread

64
Q

enzymes: evasion and damage

Hyaluronidase

A

hydrolyzes hyaluronic acid which helps hold cells together,
allowing easy spread in host tissues

65
Q

enzymes: evasion and damage

Collagenase

A

hydrolyzes collagen to allow pathogen to spread in
connective tissues

66
Q

enzymes: evasion and damage

IgA protease

A

destroys IgA antibodies produced by the host

67
Q

enzymes: evasion and damage

Hemolysins

A

lyse red blood cells to release iron for pathogen use

Microbio Test 3 Review (ch 8, 10, 11) (5 decks)

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